Home|Journals|Articles by Year Follow on Twitter

Directory for Medical Articles

Open Access

Original Article

Mouse model for myocardial injury caused by ischemia

Truc Le-Buu Pham, Dung Thi-Phuong Nguyen, Oanh Thi-Kieu Nguyen, Tam Thanh Nguyen, and Phuc Van Pham.

In the current, cardiovascular disease is one of the leading causes of death in the World. Coronary artery blockage causes acute myocardial infarction that makes myocardial tissue is damaged and can be fatal in some cases. If patients overcome the acute infarctions, the obstruction in the long run will lead to myocardial ischemia and then cell death in the ischemic myocardium area. So far there is no method to prevent effectively myocardial lesions, the development of an animal model of myocardial injury is necessary for studying new therapies for the treatment. This study aimed to create a mouse model of myocardial injury. An occluding suture of the left coronary artery in mice was made with sewing thread Prolene 7-0. That left anterior descending artery (LAD) closing caused the infarction leading to ischemia and death of cells after that. The animals were then monitored survival ratio, body weight, blood pressure and analyzed Histopathology using Hematoxylin and Eosin (H&E) stain, Trichrome stain, and Immunohistochemistry (IHC) stain to evaluate the injuries of myocardium. The results showed that six weeks after narrowing the left coronary artery, the survival percentage of the experimental group was 77% (survival 17/22), body weight and blood pressure of the experimental group (n=17) tended to decrease comparing to the control group (n=10) or heart function of the experimental group was weakening. Supporting for that result, Histopathology assessments were also showed that the damages and the death of myocardium in the experiment group. H&E stain gave the presentation that heart septum of the experimental group was thinner than the control group. Collagen formation was also observed in the experimental group by Trichrome stain results. In addition, IHC stain also indicated that the Annex-in- V (death cell marker) was expressed much stronger than those of the control group. In conclusion, the mouse model for myocardial injury caused by ischemia has been created successfully by LAD ligation.

Key words: Cardiovascular disease, Coronary arteries, Ischemia, Mouse model for myocardial injury, Myocardial infarction

Similar Articles

Exploring the Alzheimer's disease neuroepigenome: recent advances and future trends.
Zhang H, Elefant F
Neural regeneration research. 2022; 17(2): 325-327

Growth differentiation factor 5: a neurotrophic factor with neuroprotective potential in Parkinson's disease.
Goulding SR, Anantha J, Collins LM, Sullivan AM, O'Keeffe GW
Neural regeneration research. 2022; 17(1): 38-44

Presenilin mutations and their impact on neuronal differentiation in Alzheimer's disease.
Hernandez-Sapiens MA, Reza-Zaldívar EE, Márquez-Aguirre AL, Gómez-Pinedo U, Matias-Guiu J, Cevallos RR, Mateos-Díaz JC, Sánchez-González VJ, Canales-Aguirre AA
Neural regeneration research. 2022; 17(1): 31-37

Delving into the recent advancements of spinal cord injury treatment: a review of recent progress.
Flack JA, Sharma KD, Xie JY
Neural regeneration research. 2022; 17(2): 283-291

SYNGR4 and PLEKHB1 deregulation in motor neurons of amyotrophic lateral sclerosis models: potential contributions to pathobiology.
Marques RF, Duncan KE
Neural regeneration research. 2022; 17(2): 266-270

Full-text options

Add your Article(s) to Indexes
• citeindex.org

Follow ScopeMed on Twitter
Author Tools
eJPort Journal Hosting
About BiblioMed
License Information
Terms & Conditions
Privacy Policy
Contact Us

The articles in Bibliomed are open access articles licensed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (https://creativecommons.org/licenses/by-nc-sa/4.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
ScopeMed is a Database Service for Scientific Publications. Copyright ScopeMed Information Services.